Alopecia

• Jon Skalecki, M.D.

 Basic Information

Definition

Alopecia is the term used to describe involuntary hair loss, typically on the scalp but can occur anywhere over the body. Nonscarring alopecia is hair loss without clinically apparent scarring, inflammation, or skin atrophy. Scarring alopecia is characterized by permanent hair loss accompanied by tissue destruction in the form of scarring, inflammation, and/or skin atrophy.

Synonyms

1. Hair loss

2. Balding

ICD-10CM CODES
L63	Alopecia aerata
L63.0	Alopecia (capitis) totalis
L64	Androgenic alopecia
L64.0	Drug-induced androgenic alopecia
L64.8	Other androgenic alopecia
L64.9	Androgenic alopecia, unspecified
L65	Other nonscarring hair loss
L66	Cicatricial alopecia
L65.9	Nonscarring hair loss, unspecified
L63.8	Other alopecia areata
L65.0	Telogen effluvium

Epidemiology & Demographics

Incidence

Depends on etiology, for example:

1. •

   Alopecia areata affects 1% of the U.S. population by age 50 yr. There is a higher incidence at a younger age and both sexes are affected equally.

2. •

   Androgenetic alopecia affects males > females with 50% of Caucasian men affected by age 50 yr. Less common in Asians and African-American men, and often has later onset. By age 70, 40% of females are affected, with incidence increasing after menopause.

Genetics

Depends on etiology, for example:

1. •

   Androgenetic alopecia is polygenic with variable penetrance and can be inherited from one or both parents.

2. •

   Certain scarring alopecias are more predominant in people with coarser hair.

Etiology

Nonscarring

1. •

   Failure of follicle production

2. •

   Hair shaft abnormality

3. •

   Pattern hair loss, i.e., androgenetic alopecia

4. •

   Hair breakage, i.e., trichotillomania, traction alopecia, cosmetic overprocessing

5. •

   Problem with cycling (excess shedding), i.e., telogen effluvium, anagen effluvium, loose chemotherapy anagen syndrome, alopecia areata, syphilis

Scarring

1. •

   Infectious: tinea capitis with inflammation (kerion), bacterial folliculitis as in dissecting folliculitis and folliculitis decalvans

2. •

   Neoplasm: alopecia mucinosa in cutaneous T-cell lymphoma or alopecia neoplastica due to metastatic carcinoma (breast cancer)

3. •

   Autoimmune: chronic cutaneous lupus erythematosus

4. •

   Congenital

Clinical Features

History

A careful history must be taken and should include time course for hair loss, the pattern of hair loss, any recent change in life situation/stresses, any associated medical conditions, new medications, any family history of hair loss, diet, hair care practices, and other skin/nail symptoms.

Physical Examination

1. •

   General: patient’s emotional response to hair loss

2. •

   Hair/skin:

   1. 1.

      Hair thinning/loss

   2. 2.

      May have fine downy hairs also referred to as vellus hairs

   3. 3.

      Skin may show changes consistent with inflammation, infection, and/or atrophy

   4. 4.

      Women may show virilization (e.g., hirsutism)

   5. 5.

      Exclamation-point hairs can be seen in alopecia areata

   6. 6.

      Broken hairs of different length may be seen in traumatic alopecia

   7. 7.

      Hairs that crack or crumble with palpation most often signify shaft damage due to overprocessing

Diagnosis

Workup

1. •

   Pull test—no shower for 24 hr, 60 hairs are gently pulled from the scalp, removal of 6 or more hairs is considered positive result and indicates telogen effluvium (active shedding). Look for telogen bulbs on recovered hairs to differentiate from breaking (blunt ends).

2. •

   Punch biopsy—Mandatory when suspecting scarring alopecia. Send two punches: one for vertical and one for horizontal sectioning for histopathologic analysis, preferably by a dermatopathologist.

3. •

   Trichogram—quantifies hair loss. Pull 25 to 50 hairs and measure proportion of anagen to catagen and telogen hairs under light microscopy: 10% to 20% telogen hairs is normal, whereas >35% is highly suspicious for telogen effluvium.

4. •

   Fig. E1 describes the evaluation and treatment of alopecia in females.

Laboratory Tests

Initiate laboratory studies if not clear based on clinical presentation:

1. •

   CBC—rule out Fe deficiency

2. •

   Total Fe/ferritin—rule out subclinical Fe deficiency

3. •

   TSH—rule out underlying thyroid disease

4. •

   ANA—screen for autoimmune disease

5. •

   RPR—rule out cutaneous syphilis if history suggestive of increased risk

Differential Diagnosis

Nonscarring

1. •

   Telogen effluvium: This type of alopecia is usually diffuse thinning that follows significant life stress (death of loved one, high fever, severe infection, crash dieting) or change in hormones (postpartum, change in or cessation of oral contraceptives). Patient often presents with a bag of hair that has fallen out. This is caused by a large number of anagen (growing) hairs entering telogen (dying phase) simultaneously. Telogen effluvium is more common in women.

2. •

   Androgenetic alopecia: Gradual thinning of hair and a trend toward finer hair, which in men has a typical pattern of receding anterior bitemporal hairline resulting in an M-shaped pattern and hair loss at the vertex (Fig. 2) and in women has a typical pattern of thinning along vertex with or without frontotemporal thinning. This type of thinning is due to a combination of genetic predisposition and androgenic conversion of hair follicles into vellus-like follicles. Widening of the central hair part is often seen, leading to scalp visibility (Fig. 3). This female pattern of more diffuse hair loss is seen in 20% to 30% of adolescent males.

   

   

3. •

   Alopecia areata: Patches of acute hair loss (Fig. 4), typically 2 to 5 cm in diameter, with normal-appearing skin, black dots (cadaver hairs, point noir) from hair that breaks before reaching the skin’s surface, and occasional “exclamation point hairs,” which are evidence of hairs breaking off as they are pushed from the follicle. Fingernails may show fine pitting. On biopsy, lymphocytes surround the hair bulb and resemble a “swarm of bees,” evidence of the autoimmune etiology. Patients often have positive family history.AA Universalis (AAU)—generalized loss of body hairAA Totalis (AAT)—complete loss of scalp hair

   

4. •

   Tinea: This type of hair loss is evident in round patches, possibly with scarring, erythema, and lymphadenopathy. This is the most common type of hair loss in children. Diagnosis can be made by scraping the erythematous edge and placing the scraping with KOH under a microscope to check for hyphae. Wood’s lamp only fluoresces if tinea is caused by Microsporum spp.; however, the most common (in the U.S.) Trichophyton spp. does not fluoresce. If a kerion (severe alopecia associated with bogginess) is present, it may cause scarring.

5. •

   Traumatic alopecia (traction alopecia): This type of hair loss is in a pattern consistent with breaking off of hairs due to traction (hair pulling) (Fig. 5) or chemical or heating agents (hair straightening or permanent). Etiology usually becomes apparent with careful history taking and visualizing the pattern of hair loss. In trichotillomania (Fig. 6), the alopecia area has an irregular shape, scalp excoriations may present, and hairs are broken at different lengths.

   

   

Scarring

1. •

   Lichen planus: The hair loss associated with LP is typically associated with scaling and atrophy of pruritic, painful skin underlying the hair loss. This hair loss is more common in middle-aged women. While there are numerous variations in clinical presentation, the general clinical picture is one of a chronic inflammatory condition of the skin, nails, mucous membranes, and/or hair. The typical skin lesions are flat topped, violaceous lesions with white lines (Wickham’s striae), while the typical oral lesions are milky white.

2. •

   Chronic cutaneous (discoid) lupus erythematosus: This type of hair loss frequently is evident in well-demarcated, erythematous plaques in chronically sun-exposed areas of skin. Lesions exhibit hypopigmentations or hyperpigmentations, atrophy, erythema, and scaling. It may be present concurrently with SLE or be the first presenting symptom of SLE, but in most cases it is a purely cutaneous condition.

3. •

   Tinea with kerion: A kerion represents an exuberant delayed-type hypersensitivity reaction to the tinea capitis, resulting in one (or many) inflamed boggy plaque(s) on the scalp depending on the severity of the infection.

Treatment

1. •

   Telogen effluvium: Stop offending stress/medication and in 3 to 4 months anagen recurs. Hair density should be normalized by 12 months. Multiple medications have been shown to be an inciting factor and one should consider stopping them (these include, but are not limited to, enalapril, colchicine, levodopa, metoprolol, propranolol, oral contraceptives, and lithium). Full regrowth is expected in most cases.

2. •

   Androgenetic alopecia: For men, the most likely first-line treatment is oral finasteride (type II 5α-reductase inhibitor) which leads to lower levels of dihydrotestosterone. This leads to hair regrowth in about 6 months, but with cessation, hair returns to pattern of loss within 6 to 9 months. Topical minoxidil has shown similar results to finasteride and can be useful in partially restoring lost hair in both men and women. Dutasteride (off-label) has been shown to be superior to finasteride in a randomized trial but requires higher doses than that used for BPH. Discontinuation of minoxidil will result in loss of regrown hair often over several months. Other options include surgical intervention with hair transplantation or hair flaps, camouflaging agents, the use of a hairpiece, or low-level light therapy. In women with elevated androgens, antiandrogens such as spironolactone, flutamide, and cimetidine may be considered.

3. •

   Alopecia areata (AA): Spontaneous remission occurs in patchy AA, but less commonly in AAT or AAU. Glucocorticoids (GCs) are the mainstay of treatment but have little effect on the long-term outcome of hair loss—topical GC for small patches, intralesional injection of high-potency GC, and even systemic steroids can all be temporarily effective but at the cost of glucocorticoid exposure. Induction of allergic contact dermatitis using short-contact anthralin therapy or squaric acid sensitization can be effective but tends to have significant local discomfort, thereby limiting its use. Photochemotherapy has shown some beneficial outcomes, although there is a high relapse rate after discontinuation.

4. •

   Tinea capitis: To effectively treat tinea capitis, oral antifungal agents must be used. Griseofulvin is considered the drug of choice in the U.S., and the recommended time course is 6 weeks to several months. Other oral agents to consider include terbinafine, itraconazole, fluconazole, and ketoconazole. If there is a kerion (area of boggy, purulent inflammation underlying the area of hair loss), the patient is at increased risk for scarring alopecia due to bacterial superinfection, and a short course of oral steroids and oral antibiotic must be considered.

5. •

   Traumatic alopecia (traction alopecia): First priority is stopping inciting activity/agent, ideally leading to gradual resolution of hair loss and hair regrowth.

6. •

   Lichen planus: Associated hair loss is often permanent; however, for symptomatic control of itching and pain, topical or oral glucocorticoids may be considered.

7. •

   Chronic cutaneous discoid erythematosus: The best prevention is sun protection, with SPF lotion. Treatment options center around the cautious use of topical or intralesional glucocorticoids. Hydroxychloroquine and retinoids are also used with caution.

8. •

   Chemotherapy-induced alopecia: Scalp cooling devices may be effective in reducing chemotherapy-induced alopecia. In a recent trial among women with stage I to II breast cancer receiving chemotherapy with taxane, anthracycline, or both, those who underwent scalp cooling were significantly more likely to have less than 50% hair loss after the fourth chemotherapy cycle compared with those who received no scalp cooling.¹

Referral

Dermatology

Patient/Family Education

Alopecia areata: www.naaf.org

Suggested Reading

• A. Gilhar: Alopecia areata. N Engl J Med. 366:1515–1525 2012 22512484

• TG. Phillips: Hair loss: common causes and treatment. Am Fam Physician. 98 (6):371–378 2017

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